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线粒体中有多少质子?How Many Protons in a Mitochondrion?

细胞色素氧化酶反应与电镜观察结果表明人毛滴虫缺乏线粒体。It is proved that there isn't any mitochondrion in trichomonas hominis.

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但是,几乎所有那些基因完全不在线粒体的DNA中!But nearly all of those genes are not in the mitochondrion 's DNA at all!

树突肿胀、线粒体及神经微丝消失。Dendrites were swelling, in which mitochondrion and neurofilament disappeared.

只有13种线粒体的组成蛋白质是由线粒体自己的DNA编码的。Only 13 of the mitochondrion 's component proteins are encoded by its own DNA.

粗面内质网扩张,线粒体肿胀。Their rough surfaced endoplasmic reticulum was extended and mitochondrion swollen.

当线粒体老化或被自由基攻击之后,线粒体会失去活性。When aging or attacked by free radicals, the mitochondrion will be out of activity.

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线粒体是细胞内进行呼吸化学的一部机器。The mitochondrion is a machine within the cell that does the chemistry of breathing.

线粒体是细胞发生呼吸作用的主要场所,包括柠檬酸循环和氧化磷酸化两个过程。Mitochondrion is the location for cell respirations , including Krebs cycle and oxidation-phosphorylation system.

近年来发现细胞凋亡与线粒体的结构与功能有着密切的关系。At present , it is found that apoptosis have a close relation with the construction and function of mitochondrion.

视网膜内网状层线粒体产生的能量较少,表明神经节细胞活动不太活跃。The less energy produced by mitochondrion in retina's internal reticular layer shows the inactivity of the ganglion cell.

被子植物花粉发育中雄性生殖细胞中核外DNA的保存或丢失是质体和线粒体遗传的基础。Preservation or loss of extranuclear DNA introduced inherited mechanism of plastid and mitochondrion in angiosperms'pollen.

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本文主要综述了线粒体、叶绿体的内共生假说和分化假说。This paper will summarize the Endosymbiontic Hypothesis and the Intercellular origin Hypothesis of chloroplast and mitochondrion.

例如他们能精确的控制纳米管插入细胞的位置,甚至能定位到更小的细胞结构如细胞核或线粒体。They can control precisely where the nanotube penetrates a cell, for example, and een pinpoint smaller cell structures, such as the nucleus or mitochondrion.

线粒体是真核生物中拥有蛋白和酶最多的细胞器,因而隐孢子虫线粒体也可能成为药物潜在的作用靶位。Mitochondrion is an organelle which contains most protein and enzyme in eukaryotes, so the mitochondrion of Cryptosporidium may be a potential target of drugs.

结果心肌缺血-再灌注时能量耗竭、自由基形成、钙超载、细胞凋亡等过程中线粒体发挥重要的作用。Results The mitochondrion plays an crucial role in the processes of energy burn-out, free radical formation, calcium overload and cells apoptosis during myocardial ischemia-reperfusion.

目前研究表明,脑缺血再灌注后神经细胞凋亡的主要机制为线粒体损伤、钙超载及氧自由基的累积等。Many current studies have showed that the major damage mechanisms on apoptosis of the neuron are mitochondrion impairment, calcium overload, increased levels of oxygen radicals and so on.